Our findings suggest that p-STAT3 can be a functional target of PTPRD in NPC as supported by the following observations: (a) GSEA showed the significant enrichment of the Jak/STAT3 signaling pathway in NPC patients with low PTPRD expression, (b) Western blotting and IHC assays indicated a negative correlation between PTPRD and p-STAT3 in vivo and in vitro, and (c) coimmunoprecipitation and immunofluorescence assays demonstrated that PTPRD directly interacts with p-STAT3. Here, STAT3 is linked to nasopharyngeal carcinoma.